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Compare characteristics of benign and malignant neoplasms. (p.26)
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Describe 3 phases of chemical carcinogenesis. What takes place and/or influences each stage? (p.27)
- Initiation – alteration of genetic material of the cell
- o Usually result of covalent reaction between carcinogen, or some unknown factor, and DNA
- o Occurs quickly in dose-related fashion after single exposure
- o Usually affects only small number of cells
- o Occurs more frequently in rapidly proliferating tissue
- o Considered an irreversible event
- o Susceptible to promotion
- o Cancer = result of multiple mutations, NOT just one
- Promotion – initiated cells begin to express genetic changes
- o Cells begin to proliferate but growth is not yet autonomous
- o Growth seems to depend on presence of promoting stimulus
- Progression – development of tumor’s metastatic potential
- o Autonomous cell growth – independent of the promoter
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What are 3 classes of genes associated with pathogenesis of cancer? (p.25)
- Oncogenes
- Tumor suppressor genes
- DNA damage repair genes (mutator genes)
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Oncogenes
- Altered protooncogenes
- Genes that have potential to accelerate cell division
- “Gain of function” not dependent on body’s need for more cells
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Tumor suppressant genes
- Genes that slow or inhibit cell growth
- For example, if one has enough brain cells or liver cells, these cells stop cell proliferation
- Should mutations occur in these genes, cells can start to grow uncontrolled
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DNA damage repair genes
(mutator genes)
- Function to maintain integrity of normal genome
- Array of genes that function in combination to locate and repair DNA damage that may occur during replication, during normal cellular metabolism, or damage due to chemicals, viruses, radiation, etc.
- Big trouble when mutations occur in these genes – now mutations will accumulate
- If occur in tumor suppressor genes --> uncontrolled cell growth --> genomic instability = NOT good
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What are protooncogenes? (p.25)
- Genes that regulate normal cell growth and differentiation
- In most of our cells, these genes are NOT working; when we have enough cells, they turn off
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What factors have potential of transforming protooncogenes to oncogenes – genes linked to cancer?
- Mutations can activate protooncogenes to oncogenes – genes that now have potential to accelerate cell division and that “gain function”
- Not dependent on body’s need for more cells
- Mutations caused by: chemicals, viruses, free radicals, irradiation, diet-related, genetics
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What genes are associated with risk of breast cancer and ovarian cancer?
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RNA Viruses linked with development of cancer
(retrovirus)
- Human T Cell Leukemia Virus 1 (HTLV1)
- - Similar to AIDS– infects CD4 cells (helper T cells)
- - Ultimately become neoplastic transformations --> T-cell leukemia /lymphoma
- Hepatitis C – carries high risk for cirrhosis of the liver, hepatocellular carcinoma, liver failure
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DNA Viruses linked with development cancer
- Human Papillomavirus (HPV)
- - In U.S., most common STD
- - About 100 different types of papillomaviruses
- - Some associated with benign papillomas like warts on skin
- - Others associated with cervical cancer and cancer of anogenital regions
- - Also oral and layrngeal cancers
- Epstein-Barr Virus (EBV)
- - Cancers associated with this virus:
- Burkitt lymphoma (African), B-cell lymphoma (immunosuppressed individuals), Nasopharyngeal carcinoma
- Hepatitis B Virus (HBV)
- - Associated with hepatocellular carcinoma
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